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  • 1
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    Development of tetravalent IgG1 dual targeting IGF-1R–EGFR antibodies with potent tumor inhibition
    Elsevier BV ; 2012
    In:  Archives of Biochemistry and Biophysics Vol. 526, No. 2 ( 2012-10), p. 206-218
    Details
    In: Archives of Biochemistry and Biophysics, Elsevier BV, Vol. 526, No. 2 ( 2012-10), p. 206-218
    Type of Medium: Online Resource
    ISSN: 0003-9861
    URL: Article
    DOI: 10.1016/j.abb.2012.03.016
    RVK:
    WA 15000
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2012
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  • 2
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    Structural Basis for the Regulation of Insulin-like Growth Factors by IGF Binding Proteins
    Elsevier BV ; 2005
    In:  Structure Vol. 13, No. 1 ( 2005-01), p. 155-167
    Details
    In: Structure, Elsevier BV, Vol. 13, No. 1 ( 2005-01), p. 155-167
    Type of Medium: Online Resource
    ISSN: 0969-2126
    URL: Article
    DOI: 10.1016/j.str.2004.11.009
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2005
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    SSG: 12
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  • 3
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    Abstract 710: Kinetic of phosphoproteins in the PI3K and MAPK pathway reflect responsiveness of Ewing's Sarcoma cells to R1507, a human IgG1 Mab that binds IGF-IR
    American Association for Cancer Research (AACR) ; 2010
    In:  Cancer Research Vol. 70, No. 8_Supplement ( 2010-04-15), p. 710-710
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 8_Supplement ( 2010-04-15), p. 710-710
    Abstract: The Ewing Sarcoma (ES) family represents 3% of all pediatric cancers (Ludwig J.A. 2008). Following a multimodal treatment scheme ES Patients with metastases have a 5 year survival rate of less than 25% (Subbiah V. et al. 2009). For these patients, new therapy options are imperative. Specific chromosomal translocations account for 95% of all ES and lead to alteration of gene expression levels including genes up regulating IGF-IR signaling (Benini S. et al. 2004). Thus, targeting IGF-IR may be useful to interfere with tumor growth in ES. R1507 is a human IgG1 Mab that binds IGF-IR, inhibits IGF-I and II binding, leads to down modulation of the IGF-IR receptor and inhibits proliferation of cancer cells. Responsiveness to R1507 was studied in 5 ES-cell lines. RD-ES and TC71 cell lines showed maximal inhibition of tumor cell proliferation ( & gt;68%) in a 3-D, 7-days proliferation assay in vitro. MHH-ES and RH1 showed medium responsiveness (30%) but no responsiveness was observed in CADO-ES1 cells. Compared to RD-ES, CADO-ES1 harbors 5 times more insulin receptor (IR) but treatment with a combination of R1507 and IR antibody 83-14 reduced proliferation by only 11%. Thus the high expression of IR does not explain the resistance of CADO-ES1 versus R1507 treatment. Phosphorylation kinetics of 8 proteins within the Phosphoinositide 3-kinase (PI3K)-pathway and the mitogen activated protein-kinase pathway were determined with Luminex bead-based assays 0,5-50 hours after treatment with R1507. Responsive RD-ES and MHH-ES1 cell lines showed a sustained down regulation of phospho-IGF-IR (Tyr1146) by more than 80% after treatment with R1507. The non responsive CADO-ES1 cell line showed only temporary decrease of phospho-IGF-IR by 40% after 30 minutes. IRS-1 has multiple phosphorylation sites which differentially regulate the PI3K pathway. Tyrosine phosphorylation of IRS-1 initiates the PI3K signaling. Serin phosphorylation inhibits IRS-1 signaling by uncoupling IR or IGF-IR/IRS-1 interaction and inhibiting signal transduction via tyrosine phosphorylation. After treatment with R1507, tyrosine phosphorylation of IRS-1 was decreased in responsive cell lines by 60% but phosphorylation of Ser636/Ser639 was increased 2,5-fold. To analyze this effect in more detail, a panel of 13 human tumor cell lines was analyzed. Correlation of increased Ser636/Ser639 IRS-1 phosphorylation and responsiveness towards R1507 was observed in most cell lines. Furthermore in responsive cell lines a 60% reduction of phospho-Akt (Ser473) and phospho-p70S6kinase (Thr421/Ser424) can be observed. In contrast no effect on phosphorylation status for IRS-1, Akt and p70S6 kinase was observed in non responsive cell line CADO-ES1. In conclusion the kinetic of phosphoproteins and especially the phosphorylation status of IRS-1 might be indicative for sensitivity of cancer cells to IGF-IR targeting reagents. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 710.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM10-710
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
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  • 4
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    R1507, an Anti-Insulin-Like Growth Factor-1 Receptor (IGF-1R) Antibody, and EWS/FLI-1 siRNA in Ewing's Sarcoma: Convergence at the IGF/IGFR/Akt Axis
    Public Library of Science (PLoS) ; 2011
    In:  PLoS ONE Vol. 6, No. 10 ( 2011-10-11), p. e26060-
    Details
    In: PLoS ONE, Public Library of Science (PLoS), Vol. 6, No. 10 ( 2011-10-11), p. e26060-
    Type of Medium: Online Resource
    ISSN: 1932-6203
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    DOI: 10.1371/journal.pone.0026060
    DOI: 10.1371/journal.pone.0026060.g001
    DOI: 10.1371/journal.pone.0026060.g002
    DOI: 10.1371/journal.pone.0026060.g003
    DOI: 10.1371/journal.pone.0026060.g004
    DOI: 10.1371/journal.pone.0026060.g005
    DOI: 10.1371/journal.pone.0026060.t001
    DOI: 10.1371/journal.pone.0026060.s001
    Language: English
    Publisher: Public Library of Science (PLoS)
    Publication Date: 2011
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  • 5
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    R1507, a Monoclonal Antibody to the Insulin-Like Growth Factor 1 Receptor, in Patients With Recurrent or Refractory Ewing Sarcoma Family of Tumors: Results of a Phase II Sarcoma Alliance for Research Through Collaboration Study
    American Society of Clinical Oncology (ASCO) ; 2011
    In:  Journal of Clinical Oncology Vol. 29, No. 34 ( 2011-12-01), p. 4541-4547
    Details
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 29, No. 34 ( 2011-12-01), p. 4541-4547
    Abstract: The type 1 insulin-like growth factor 1 receptor (IGF-1R) has been implicated in the pathogenesis of the Ewing sarcoma family of tumors (ESFT). We conducted a multicenter phase II study of the fully human IGF-1R monoclonal antibody R1507 in patients with recurrent or refractory ESFT. Patients and Methods Patients ≥ 2 years of age with refractory or recurrent ESFT received R1507 at doses of 9 mg/kg intravenously one a week or 27 mg/kg intravenously every three weeks. Response was measured by using WHO criteria. Tumor imaging was performed every 6 weeks for 24 weeks and then every 12 weeks. Results From December 2007 through April 2010, 115 eligible patients from 31 different institutions were enrolled. The median age was 25 years (range, 8 to 78 years). The location of the primary tumor was bone in 57% of patients and extraskeletal in 43% of patients. A total of 109 patients were treated with R1507 9 mg/kg/wk, and six patients were treated with 27 mg/kg/3 wk. The overall complete response/partial response rate was 10% (95% CI, 4.9% to 16.5%). The median duration of response was 29 weeks (range, 12 to 94 weeks), and the median overall survival was 7.6 months (95% CI, 6 to 9.7 months). Ten of 11 responses were observed in patients who presented with primary bone tumors (P = .016). The most common adverse events of grades 3 to 4 were pain (15%), anemia (8%), thrombocytopenia (7%), and asthenia (5%). Conclusion R1507 was a well-tolerated agent that had meaningful and durable benefit in a subgroup of patients with ESFT. The identification of markers that are predictive of a benefit is necessary to fully capitalize on this approach.
    Type of Medium: Online Resource
    ISSN: 0732-183X , 1527-7755
    URL: Article
    DOI: 10.1200/JCO.2010.34.0000
    RVK:
    XA 52760
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2011
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  • 6
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    Abstract LB-397: Functional characterization of IGF-1R antibodies and possible implications for clinical safety and efficacy
    American Association for Cancer Research (AACR) ; 2011
    In:  Cancer Research Vol. 71, No. 8_Supplement ( 2011-04-15), p. LB-397-LB-397
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 71, No. 8_Supplement ( 2011-04-15), p. LB-397-LB-397
    Abstract: Background This is the first study performing a head to head comparison of monoclonal IGF-1R antibodies (mAb) based on published sequences for therapeutic mAbs from Pfizer (CP751,871, IgG2 kappa), Amgen (AMG479, IgG1 lambda), Merck (h7C10, cloned to R1507 backbone), Imclone (IMC-A12, IgG1 lambda) and Roche (R1507, IgG1). Methods In this study, sequence information for IGF-1R mAbs was extracted from patents and used to clone and transiently express IgGs (*=re-synthesized) in HEK293F cells. In vitro assays for ligand binding, IGF-1R auto-phosphorylation, IGF-1R downregulation, IR co-downregulation, and affinity analyses (Biacore) were used. In vivo comparison was done in BxPC3 xenograft mouse model. Results All antibodies inhibit IGF-1 binding and signaling at low nanomolar levels. While IMC-A12* and R1507 also prevent IGF-2 binding to IGF-1R and subsequent receptor activation, CP751,871* and h7C10* do not inhibit IGF-2 binding and have only limited impact (55%/30% inhibition) on IGF-2 signaling. Analysis of IGF-1R phosphorylation in 0.5 % FCS medium revealed that all antibodies except R1507 exert agonistic activity. Interestingly, Fab fragments of agonistic mAbs became antagonistic, indicating that bivalent binding is necessary for agonistic effects. All mAb (200nM, 24h treatment of MCF-7 cells) with the exception of AMG479* efficiently downregulated 78–82% the IGF-1R. Analysis of the same cell lysates revealed however striking differences in IR co-downregulation, a mechanism discussed as possible cause of clinical hyperglycemia. R1507 had the least side effects on Insulin co-downregulation (9%) compared to h7C10* (15%), CP751,871* (23%) and IMC-A12* (46%). Differences were also seen in the binding kinetics. Both AMG479* and R1507 showed faster koff rates resulting in shorter retention times at the receptor. Since kon/koff rates are discussed to influence tumor penetration (1), we compared downregulation of IGF-1R by R1507 and CP751,871* in xenograft tumors. Although both mAbs downregulate IGF-1R in vitro to the same extent, R1507 was significantly more effective in the in-vivo setting. Conclusion The head to head comparison of IGF-1R mAbs revealed differences in regard to binding properties, tumor penetration, IR codownregulation, and inhibition of signaling via the ligand IGF-2. Reference List 1. Adams, G. P., Schier, R., McCall, A. M., Simmons, H. H., Horak, E. M., Alpaugh, R. K., Marks, J. D., and Weiner, L. M. (2001) Cancer Res. 61, 4750–4755 Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr LB-397. doi:10.1158/1538-7445.AM2011-LB-397
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2011-LB-397
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2011
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  • 7
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    Abstract 1755: Sensitization of radiotherapy and chemotherapy by adjunction of R1507 (anti-IGF-1R monoclonal antibody) in small cell lung cancer cell lines: Opportunity of translating the triple combination R1507-Cisplatin-radiotherapy
    American Association for Cancer Research (AACR) ; 2011
    In:  Cancer Research Vol. 71, No. 8_Supplement ( 2011-04-15), p. 1755-1755
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 71, No. 8_Supplement ( 2011-04-15), p. 1755-1755
    Abstract: Introduction: Insulin like growth factor receptor-1 (IGF-1R) inhibition could be a pertinent therapeutic approach in small cell lung cancer (SCLC), given the recognized activation of an IGF-1R autocrine loop. Materials and methods: We evaluated the importance of IGF-1R axis in SCLC by assessing IGF-1R expression and Akt activation in 83 human SCLC tissue specimens. In parallel, we evaluated in vitro the efficacy of R1507, an IgG1 fully human monoclonal antibody directed to IGF-1R. R1507 effects on IGF-1R and downstream pathways were assessed using three SCLC cell lines: H69, H146 and H526. The cytotoxicity of R1507, Cisplatin and ionizing radiation (IR) was evaluated by WST-1 cell proliferation assays and clonogenic survival assays. In vivo, the efficacy of R1507, Cisplatin and IR was assessed on H526 and H146 xenografts in nude mice. Results: IGF1R was overexpressed and Akt was activated in 38 (46%) and 31 (37%) of 83 SCLC tumors, respectively. In vitro, R1507 down-regulates IGF-1R receptor and disrupts downstream signaling through Akt and MAPK pathways in a dose dependent manner in selected small cell lung cancer cell lines. R1507 inhibits cell proliferation and colony forming capacity in H526 and H146 cells but not in H69 cells. The inhibition of PI3K-Akt pathway correlated with treatment response. The combination of R1507 (200 nM) and CDDP (3 μM) exhibited a synergistic inhibitory effect on the colony forming capacity of H146 cells and an additive inhibitory effect on H526 cells. R1507 showed synergistic effects with IR (2 Gy) in H146 cells and an additive inhibitory effect in H526 cells. R1507 potentiates the IR effects and induces a prolonged increase of the proportion of sub G1 cells in H526 but not in H146 cell line. The triple combination R1507-Cisplatin-IR potentiates the antitumoral effect of Cisplatin-IR (current standard treatment) in H146 and in H526 cell lines. In vivo, R1507 administered in monotherapy leads to a non-significant delay of tumor growth in H526 xenografts but sensitizes to both Cisplatin and IR. The triple combination R1507-Cisplatin-IR achieves a long lasting delay in tumor growth as compared with the current standard treatment Cisplatin-IR. Conclusion: R1507 has a single agent activity and remarkable chemo- and radiosensitizing effect in defined SCLC cell lines in vitro. Efficacy is dose-dependent and related to the capacity to inhibit PI3K-Akt signaling pathway. In vivo, it sensitizes to both IR and Cisplatin effects. The triple combination R1507-Cisplatin-IR exhibits a long lasting tumor growth delay as compared with the current standard treatment Cisplatin-IR, the potential of this combination should be evaluated in further early clinical trials. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1755. doi:10.1158/1538-7445.AM2011-1755
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2011-1755
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2011
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  • 8
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    Abstract LB-212: XGFR, an Fc-engineered dual signaling inhibitor targeting IGF-1R and EGFR
    American Association for Cancer Research (AACR) ; 2011
    In:  Cancer Research Vol. 71, No. 8_Supplement ( 2011-04-15), p. LB-212-LB-212
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 71, No. 8_Supplement ( 2011-04-15), p. LB-212-LB-212
    Abstract: Background: Elevated signaling via the receptor tyrosine kinases IGF-1R and EGFR has been identified as common characteristic of multiple cancer type. IGF-1R and EGFR signal predominantly through the PI3K and MAPK signaling pathways and thereby mediate growth and survival signals crucial for the development and progression of cancer. There is strong cross talk on multiple levels between IGF-1R and EGFR dependent signaling pathways. Therefore, targeting IGF-1R and EGFR simultaneously is an attractive way to achieve maximal inhibition of signal transduction and to avoid resistance formation. Methods: Bispecific IGF1R-EGFR antibodies were engineered by linking scFv domains of an EGFR Mab (GA201) via Serine-Glycine linkers to an IgG1 IGF-1R Mab (RG1507). The functional properties of the bispecific antibodies were evaluated in cellular in vitro assays (IGF-1R/EGFR phosphorylation, downregulation, 3D proliferation and ADCC assays) and in in vivo xenograft models for tumor growth inhibition and survival. Results: Bispecific IGF-1R-EGFR antibodies (XGFR2, XGFR3, XGFR4) were successfully generated with yields and stability comparable to conventional IgG1 antibodies. XGFR antibodies effectively inhibited IGF-1R and EGFR phosphorylation and 3D proliferation in H322M tumor cells and induced strong downmodulation of IGF-1R and enhanced EGFR downmodulation compared to the parental EGFR antibody GA201. XGFR antibodies showed strong anti-tumor efficacy comparable to the combination of monospecific IGF-1R and EGFR Mabs in the BxPC3 and H322M xenograft models. To enhance the ADCC properties of XGFR, afucosylated, glycoengineered bispecific antibodies with enhanced affinity for FcγRIIIA were generated using the GlycoMab technology. Glycoengineered bispecific antibodies were shown to have superior ADCC properties in in vitro ADCC assays and XGFR4 significantly prolonged median and overall survival of mice in an ADCC competent in vivo model (A549 i.v.). Conclusions: Bispecific IGF-1R-EGFR antibodies represent an attractive therapeutic strategy to simultaneously target two key components of multiple cancer types (IGF-1R and EGFR), resulting in effective inhibition of the PI3K and MAPK signaling pathway and to avoid the formation of resistance to therapy. Having overcome issues of stability and productivity, bispecific antibodies may become an advantageous way to reduce costs and infusion times in cancer therapy, while at the same time, achieving maximal anti-tumor effects through inhibition of multiple targets. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr LB-212. doi:10.1158/1538-7445.AM2011-LB-212
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2011-LB-212
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2011
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  • 9
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    Abstract 2051: BI 905711, a novel CDH17-targeting TRAILR2 agonist, effectively triggers tumor cell apoptosis and tumor regressions selectively in CDH17-positive colorectal cancer models
    American Association for Cancer Research (AACR) ; 2019
    In:  Cancer Research Vol. 79, No. 13_Supplement ( 2019-07-01), p. 2051-2051
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 79, No. 13_Supplement ( 2019-07-01), p. 2051-2051
    Abstract: The tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) has the capability to induce apoptosis in a wide variety of tumor cells and has emerged as an important therapeutic concept for cancer treatment. To date however, TRAILR2 agonistic antibodies, designed to trigger tumor cell apoptosis, have only had limited clinical success due either to lack of efficacy or liver toxicity. BI 905711, a tetravalent bispecific antibody targeting both TRAILR2 and CDH17, was designed to overcome the disadvantages of current TRAILR2 antibodies. CDH17-dependent clustering of TRAILR2 permits BI 905711 to selectively induce apoptosis in CDH17-expressing tumor cells. CDH17 was selected as the anchor target due to its restricted expression, in particular a lack of expression in normal liver tissue, thereby avoiding the clinical hepatotoxicity associated with TRAILR2 agonism. Here, we report the preclinical activity of BI 905711 using colorectal cancer (CRC)-derived cell lines and patient-derived xenograft (PDX) models. We demonstrated that BI 905711 effectively triggered apoptosis in a broad range of CDH17-positive CRC tumor cells in vitro. Furthermore, BI 905711 potently initiated the apoptosis cascade as evidenced by a strong post-treatment increase of both caspase-8 and caspase-3/7. Importantly, induction of extrinsic apoptosis signaling by BI 905711 was strictly CDH17-dependent, as further demonstrated using a pair of CDH17-positive and -negative clones of the CRC cell line GP2d. When comparing the CDH17-negative clone with the parental cell line, the absence of CDH17 translated into a more than 1000-fold drop in BI 905711-dependent efficacy. Moreover, BI 905711 demonstrated single-agent tumor regressions in the GP2d colorectal cancer xenograft model. The antitumor efficacy of BI 905711 was further investigated in vivo in different CRC PDX models, showing effective tumor growth inhibition in a q14d dosing schedule. In summary, we demonstrated that BI 905711 potently triggers the extrinsic apoptosis pathway specifically in CDH17-positive tumor cells, which translates into significant tumor growth inhibition in CRC patient-derived xenograft tumors. BI 905711 is a first-in-class molecule that shows superiority to existing TRAILR2 agonists, represents a targeted strategy for the treatment of CRC and additional CDH17-positive cancer types. Together with its potential for a favorable safety profile, these data support our plan for a phase I trial of BI 905711 in these patient populations. Citation Format: Juan Manuel Garcia-Martinez, Andreas Wernitznig, Joerg Rinnenthal, Maria Antonietta Impagnatiello, Frank Hilberg, Craig Giragossian, Norbert Kraut, Mark Pearson, Klaus-Peter Kuenkele. BI 905711, a novel CDH17-targeting TRAILR2 agonist, effectively triggers tumor cell apoptosis and tumor regressions selectively in CDH17-positive colorectal cancer models [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 2051.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2019-2051
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2019
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